Effect of Nanoplasics on Neural Health
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Nanoplastics (NPs) are plastic particles of size less than 1um. They are commonly found in marine environments, but have been increasingly exposed to humans through cosmetics, synthetic clothing, plastic litter, ingestion of nanoplastic-exposed organisms, or even table salt. Although there is documented research on the effects of nanoplastics on aquatic organisms, little research exists on the impact of NPs, if any, on humans.
Aim: To measure the cellular effects of nanoplastics on human motor neurons in terms of protein stress markers.
Method: An in-vitro neural model comprising of human motor neurons (MNs) was obtained by differentiating the ReNVM neural progenitor cell line. MNs were then exposed to fluorescent nanopolystyrene particles of sizes 50nm, 500nm, and 5um and to two controls comprising of no NPs and of 50nm-COOH particles for 2 hours. Samples were imaged and analysed for Endoplastic-Reticulum (ER) stress, autophagy (cell destruction), senescence (diminished cell division), and inflammation genetic markers at 24, 48, 72, 96, and 120 hours post-exposure.
Results: Results showed elevated gene expression for each of the aforementioned markers in the non-control conditions at 72 hours post-exposure, but no notable rise in gene markers was found before 72h. In particular, the CHOP and CXCL8 markers for apoptosis (cell death) and inflammation were significantly higher as compared to control conditions. Results were consistent across repeats, and were supported by visible blebbing (formation of bulges) in motor neurons, a marker for cell apoptosis, in the fluorescent images taken. (See images and gene expression marker results here.)
Conclusion: These results suggest that, in addition to oxidative stress as shown by previous studies, nanoplastics induce proteostatic stress on human motor neurons, resulting in cells resorting to autophagy, senescence, inflammation and apoptosis in order to cope with the accumulated proteins. Possible alternative mechanisms for the results obtained, as well as future investigations, are also discussed.
In all, this understanding brings us one step closer to deconstructing the implications of accelerating nanoplastic pollution for neurotoxicity in humans.